Borrelia Ebook

Lyme Strategies

By Fernando Mitchell on Thu, 06 Sep 2018

This latest updated text, in digital eBook form and available for immediate download, has been expanded nearly eightfold over the original guide of 2004 in terms of the exact, step-by-step lue-print and essential information designed to maximize this protocol. Just some of the valuable information contained in this 193-page guide includes: How to do the protocol, including the exact, specific method or procedure that is critical to its success. Schedule chart, measurements guide, tips and recommendations. The basic elements of the protocol are actually five, not just salt and vitamin C what these are and why Understanding what a Jarisch-Herxheimer reaction (or Herx) is. Particular djunct items found to be extremely helpful and particular items for special issues. A Technical Section detailing why the protocol works (posited mechanisms), including scientific citations and and studies. The right salt versus wrong salt and why. the low-salt, no-salt myth and scientific truth. the historical, medicinal use of natural salt. Did you know salt was used to treat syphilis, caused by Lyme's bacterial cousin, in the 1800s? Why Vitamin C and what does it do? The protocol and specific body considerations (heart, adrenals, etc.) Key Characteristics of the Lyme bacterium (Borrelia burgdorferi), including nearly 20 extraordinary mechanisms and features it uses to elude the immune and proliferate in the body

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Contents: 193 Pages EBookAuthor: M. FettPrice: $29.95

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Existing and potential management strategies for the control of Lyme borreliosis. These approaches may reduce exposure to the tick vector, target the tick vector or target the pathogen. Vaccination against Borrelia burgdorferi. Early diagnosis and treatment of infection. Research into immunological interactions of the tick-host-pathogen interface. Development of anti-tick vaccines. Vegetative modifications (mowing, clearing leaves, xeric substrates) and burning to render the environment less suitable for tick survival and for tick hosts. Use of pheromone-based lures and decoys with acaricides for tick control, either on or off host. Concepts of IPM related to ticks and vector-borne disease and application of IPM strategies. Use of computer models to simulate various strategies for the prevention of Lyme borreliosis. line of defence in the prevention of LB. These include avoidance and reduction of time spent in tick-infested habitats, using protective clothing and tick...

Of the 11 known members of the B. burgdorferi s.l. species complex (Table 3.1), only three, B. burgdorferi s.s., B. afzelii and B. garinii, are known to be pathogenic in humans, but there are also unknown types of B. burgdorferi s.l. isolated from LB patients and the species defining process is still going on (Picken et al., 1996 Strle et al., 1997 Wang, G. et al., 1999a). Classification of the relapsing fever spirochaetes was based on the different argasid tick vectors involved the 'one tick vector species - one Borrelia species' concept. This approach for the classification of LB spirochaetes transmitted by ixodid ticks of the I. ricinus species complex (see Eisen and Lane, Chapter 4) was abandoned when it became

Numerous B. burgdorferi s.l. strains have been isolated and even more PCR fragments have been amplified from various sources. In order to determine the Borrelia species present in the samples several genotypic and phenotypic methods have been developed. Variations in the rDNA and its intergenic spacer have been used to develop different typing systems for Borrelia strains and DNA. These ribotyping methods are commonly used since they are easy to perform on both cultivated strains and B. burgdorferi s.l. DNA isolated from various sources. Analysis of restriction fragment length polymorphisms and sequencing of 16S rDNA, 23S rDNA and the intergenic spacer between the duplicated 23S and 5S rRNA genes have also been very useful in phylogenetic studies of B. burgdorferi s.l. (Marconi and Garon, 1992b Postic et al, 1994).

To increase their chances of transmission by an arthropod from one host to another, borreliae persist in the host for as long as possible. Persistence can be achieved by a mechanism called antigenic variation, and this mechanism has been studied for several years in relapsing fever borreliosis where new serotypes appear during relapses as a change in novel surface proteins called variable major proteins (Vmps). In the relapsing fever spirochaete B. hermsii, at least 26 different surface-exposed lipoproteins encoded by genes situated on linear plasmids are alternately expressed and presented, one at a time, on the bacterial surface In B. burgdorferi s.s a 28 kb linear plasmid was found to have a vmp-like sequence (vls locus) that resembles the Vmp system in B. hermsii (Zhang et al., 1997). Fifteen non-expressed vls cassettes can be recombined into a functional and expressed vlsE region resulting in antigenic variation of the expressed lipoprotein (Zhang et al., 1997) and involving...

In relapsing fever spirochaetes such as Borrelia hermsii, recombination generates new variable membrane protein (vmp) genotypes in the course of infection. New genotypes that are not yet recognized by the host are positively selected, which leads to a temporarily high spirochaetaemia that is later cleared by strong Fig. 5.1. Midpoint rooted maximum likelihood tree based on ospA sequences derived from Ixodes uriae ticks (shown in bold), various Borrelia burgdorferi s.l. isolates, and sequences downloaded from GenBank (indicated with an asterisk *). Bootstrap values under 70 are not shown. The bar indicates nucleotide substitutions per site. Fig. 5.3. Midpoint rooted maximum likelihood tree based on ospC sequences derived from a pelagic habitat (shown in bold), various terrestrial Borrelia burgdorferi s.l. isolates, and sequences downloaded from GenBank (indicated with an asterisk). Bootstrap values below 70 are not shown. The bar indicates nucleotide substitutions per site. This gene...

Borreliae are thin, elongated, motile, wave-like bacteria (Fig. 3.1). A general feature of the spirochaetes, including B. burgdorferi s.l., is that they possess a fragile outer membrane surrounding the protoplasmic cylinder. This cylinder consists of a peptidoglycan layer, a cytoplasmic membrane (inner membrane) and the enclosed cytoplasmic contents (Johnson et al., 1984 Barbour and Hayes, 1986). The outer cell membrane is fluid and consists of 45-62 protein, 23-50 lipid and 3-4 carbohydrate (Barbour and Hayes, 1986). The borreliae have 7-11 bipolar flagella located in the periplasmic space where they are attached to the poles and wrapped around the cell cylinder, giving the bacterium its characteristic flat wave shape (Barbour and Hayes, 1986 Goldstein et al., 1994 Motaleb et al., 2000). Unlike other bacterial flagella, those of the spirochaetes are endoflagella, located in the periplasmic space between the protoplasmic cylinder and the outer cell membrane and attached to the poles...

Furthermore, in another study we have demonstrated that B. burgdorferi s.l. can persist for several months in passerine birds and the infection in redwing thrushes can be reactivated in response to migration (Gylfe et al., 2000). Thus, birds may be more infectious to ticks during their migration and therefore important long-range disseminators of B. burgdorferi s.l. This work shows that migrating seabirds and passerine birds are probably important for the long-range dispersal of B. burgdorferi s.l. and that this mechanism of dispersal could be important for the distribution of human Lyme disease. Using similar approaches, other researchers have demonstrated the relative importance of different animals as reservoir hosts for different B. burgdorferi s.l species in Europe. For example, since Borrelia valaisiana has only been isolated from birds, birds have been implicated as being the only reservoir for this Borrelia species (Kurtenbach et al., 1998). B. afzelii, on the other hand, is...

Although the treponemes and borreliae exhibit a lot of similarities, a striking difference is their genome organization and structure. The members of the genus Borrelia have a very unusual genome organization among prokaryotic organisms as they have a polyploid genome that is mostly linear. The small linear replicons in borreliae have been called plasmids but, as in the genus Trypanosoma, there is justification for designating them mini chromosomes instead. A comparison of the ends of these replicons, i.e. the telomeres, with telomeric sequences of other linear double-stranded DNA replicons revealed sequence similarities with poxviruses, especially with the iridovirus agent of African swine fever. Interestingly, the latter virus and a relapsing fever Borrelia sp., Borrelia duttoni, share the same tick vector. These findings suggest that the linear replicons of B. burgdorferi s.l. originated through a horizontal gene transfer across the kingdom. Since this structural feature is found...

Borrelia burgdorferi sensu lato stained by indirect immunofluorescence using the flagellin (FlaB) antibody H9724. (Photo courtesy of Bj rn Olsen.) Fig. 3.1. Borrelia burgdorferi sensu lato stained by indirect immunofluorescence using the flagellin (FlaB) antibody H9724. (Photo courtesy of Bj rn Olsen.) Goldstein et al., 1996). Each PF is attached at only one end and in Borrelia spp. they are long enough to overlap in the centre of the cell (Johnson et al., 1984). The genes encoding the flagellar proteins are flaA (Ge and Charon, 1997a), flaB (Wallich et al, 1990), flgE (Jwang et al, 1995), fliH and fliI (Ge et al, 1996), and the flgK operons (Ge et al., 1997), and are located on the chromosome. These genes have homologies to various genes in the flagellar apparatus of both animal and plant pathogens. This suggests that the flagellar apparatus and its protein export pathways are well conserved. Swimming B. burgdorferi s.l. cells have a flattened wave-like shape similar to...

This is based on the observation that biosynthetic labelling of borrelia cultures with 14C -amino acids identified only a few amphiphilic polypeptides that do not co-migrate with lipoproteins (Brandt et al., 1990). It was also shown that these putative transmembrane proteins were in relatively low abundance when visualized by freeze-fracture electron microscopy (Walker et al., 1991 Radolf et al., 1994). Virtually none of the proteins were recognized by sera from patients with chronic LB (Brandt et al., 1990). Thus, B. burgdorferi s.l. contains two classes of integral membrane proteins abundant lipoproteins and rare transmembrane-spanning proteins.

The aim of this chapter has been to describe the current status of the molecular and cellular biology of LB spirochaetes. Much of this recent knowledge is directly coupled to the published genome sequence of B. burgdorferi s.s. B31. The new genomics and proteomics era that we have entered will be instrumental for future understanding of B. burgdorferi s.l. In addition, the combination of data from other microorganisms also has the potential of further increasing knowledge of the biology of Borrelia spp. spirochaetes in general and their pathogenesis in particular. The approach in the future will be to identify the central regulators of common host responses and the manner in which Borrelia spp. spirochaetes attempt to defeat this process. This should lead to the development of valuable tools for designing novel prophylactic and diagnostic methods.

Until recently, genetic studies in Borrelia spp. have been hindered by the lack of an exogenous selectable marker, low transformation frequency and difficulties in growing B. burgdorferi s.l. on solid medium. The first selectable marker used for B. burgdorferi s.l. was gyrBr, a mutated form of the chromosomal gyrB gene, which encodes the B subunit of DNA gyrase and confers resistance to the antibiotic coumermycin A1 (Samuels et al., 1994a,b). The use of coumermycin as a selectable marker is limited by a high frequency of recombination with the endogenous gyrB gene. A major improvement was made when Bono et al. (2000) developed an efficient marker for mutant selection in B. burgdorferi s.l. By linking the B. burgdorferi flaA or flgB promoter with the kan gene from Tn903, transformants were resistant to high levels of kanamycin. With this innovation the pace of gene inactivation will increase, and genes that have been inactivated in B. burgdorferi s.l. and published are shown in Table...

Various studies have attempted to identifiy the mechanisms that confer resistance to complement in the Borrelia system. All B. burgdorferi s.l. strains invariably bind C3. It is now established that resistant and sensitive strains differ with respect to deposition of C5b-C9, the membrane attack complex. As already described, resistance to complement is mediated by species-specific binding of two complement control proteins factor H-like protein 1 reconectin and factor H. Species-restricted binding of complement control proteins is mediated by Table 5.1. Resistance of Borrelia burgdorferi sensu lato to host complement.

Information on exposures to environmental agents can be used in evaluating the risk to health represented by noninfectious diseases, injuries, and certain infectious diseases. For example, measurement of airborne particulates is useful in assessing risks related to certain pulmonary disorders (e.g., asthma and lung cancer). Information on vectors that may carry agents of infectious disease (e.g., ticks as vectors for Lyme disease and Rocky Mountain spotted fever, mosquitoes as vectors for viral encephalitides, and raccoons as vectors for rabies) is important in evaluating the risk of infection. Information on exposures to known risks supports the development and implementation of rational public health interventions (e.g., ATSDR's Hazardous Substances Emergency Events Surveillance System provides information on the public health consequences associated with the release of hazardous substances) (CDC 1994e). In addition, information on exposures provides the basis for issuing alerts to...

Chronic fatigue syndrome (CFS) A severely disabling fatigue with self-reported impairments in concentration and short-term memory, sleep disturbances and musculoskeletal pain. Occurs worldwide. A number of infectious agents have been proposed as etiologic agents of CFS, including Human herpesviruses 4 (EBV), 5 (CMV) and 6 (HHV6) enteroviruses retroviruses and Borrelia burgdorferi. None has proved to be a unique causative agent, but it remains possible that such infections act as a trigger for the syndrome. Synonyms post-viral fatigue syndrome myalgic encephalitis (ME).

Borrelia Burgdorferi (Lyme disease) Clinical syndrome signs The earliest stage of Lyme disease (stage I) is characterized by the unique skin rash and symptoms of general infection. Neuroborreliosis begins in stage II of the disease. Pathogenesis Lyme disease (sometimes known as Bannwarth's syndrome in Europe) is caused by infection with the Borrelia Burgdorferi spirochete. The infection is transmitted by bites from the Ixodes dammini, scapularis, and pacificus tick species. The cause of peripheral neuropathy following infection is unclear, although there is cross reactivity between spirochete antigens and epitopes from Schwann cells and PNS axons.

The blacklegged tick was detected in mice on the four islands that had no deer. This suggested that, in the absence of deer, other mammalian hosts could not sustain the tick in sufficient numbers to transmit the LB or babesiosis agents. However, a population of the bird-feeding Ixodes uriae and Borrelia garinii were maintained on a Baltic island and on the Faeroe Islands where marine birds were the only vertebrate host, demonstrating that deer and or other mammals are not a prerequisite for completion of the life cycle and transmission of B. burgdorferi s.l. (Olsen et al., 1993 Gylfe et al., 1999).

A variety of environmental factors have been proposed as etiologic or modifying agents. Classical tics can be exacerbated by external factors (stress, anxiety, and fatigue), elevations of temperature, infections, and the use of other medications.9,10,25 Postulated predisposing factors include low birth weight, conditions influencing intra-uterine growth,26 exposure to medications or illicit drugs,27,28 hyper-thermia,29,30 and infections.31-34 A hypothesized role for infections, especially streptococcal infections, as a primary etiology for tics has been suggested for many years.31,35-38 Proposals of relationships between tics and infectious agents are not, however, limited to Group A b-hemolytic streptococcal (GABHS) infection. Typical symptoms of TS have also been reported in isolated cases following acute infections with Streptococcus pyogenes, lyme borreliosis, and Mycoplasma pneumoniae,33,34,39 and exacerbations have followed common colds.40 Individuals may also have multiple...